Effect of intestinal inflammation on capsaicin-sensitive afferents in the ileum of Schistosoma mansoni -infected mice

Jonge, F De; Nassauw, Luc Van; Adriaensen, Dirk; Meir, F. van; Miller, H. R. P.; Marck, Eric Van; Timmermans, Jean‐Pierre

doi:10.1007/s00418-003-0532-5

Cited by 50 publications

(55 citation statements)

References 38 publications

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“…51 CGRP has also been reported to exert chemotactive effect and promote mast cells recruitment. 62 In our study, CGRP blockade does not reverse the protective effect of exogenous PAR 2 activation in intestinal ischemia, suggesting rather a proinflammatory role of CGRP. 31 By contrast, in view of the increased damage score in SO rats pretreated with CGRP 8 -37 compared with saline SO rats, we cannot exclude a protective role of CGRP in mild inflammatory status, as induced by laparotomy and intestinal manipulation.…”

Section: Discussionmentioning

confidence: 77%

Protective Effect of Proteinase-Activated Receptor 2 Activation on Motility Impairment and Tissue Damage Induced by Intestinal Ischemia/Reperfusion in Rodents

Cattaruzza

Cenac

Barocelli

et al. 2006

The American Journal of Pathology

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We hypothesized that proteinase-activated receptor-2 (PAR 2 ) modulates intestinal injuries induced by ischemia/reperfusion. Ischemia (1 hour) plus reperfusion (6 hours) significantly delayed gastrointestinal transit (GIT) compared with sham operation. Intraduodenal injection of PAR 2 -activating peptide SLIGRL-NH 2 significantly accelerated transit in ischemia/reperfusion but not in sham-operated rats. GIT was significantly delayed in ischemia/reperfusion and sham-operated PAR 2 ؊/؊ mice compared with PAR 2 ؉/؉ . SLIGRL-NH 2 significantly accelerated transit in ischemia/reperfusion in PAR 2 ؉/؉ but not in PAR 2 ؊/؊ mice. Prevention of mast cell degranulation with cromolyn, ablation of visceral afferents with capsaicin, and antagonism of calcitonin generelated peptide (CGRP) and neurokinin-1 receptors with CGRP 8 -37 and RP67580, respectively, abolished the SLIGRL-NH 2 -induced stimulatory effect on transit in ischemia/reperfusion. Tissue damage was significantly reduced by SLIGRL-NH 2 ; this effect was not observed in cromolyn-, capsaicin-, or RP67580-treated rats but was detected following CGRP 8 -37 . Intestinal PAR 2 mRNA levels were not affected by SLIGRL-NH 2 in ischemia/reperfusion. We propose that PAR 2 modulates GIT and tissue damage in intestinal ischemia/reperfusion by a mechanism dependent on mast cells and visceral afferents. PAR 2 effect on transit might be mediated by CGRP and substance P, whereas the effect on tissue damage appears to involve substance P but not CGRP. PAR 2 might be a signaling system in the neuroimmune communication in intestinal ischemia/reperfusion.

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Section: Discussionmentioning

confidence: 77%

Protective Effect of Proteinase-Activated Receptor 2 Activation on Motility Impairment and Tissue Damage Induced by Intestinal Ischemia/Reperfusion in Rodents

Cattaruzza

Cenac

Barocelli

et al. 2006

The American Journal of Pathology

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“…Based on previous studies in the mouse by our group and others and the limited IR in perikarya, these fibers are presumed to originate extrinsically in the spinal and vagal ganglia (De Jonge et al 2003;Ward et al 2003;Matsumoto et al 2011). The intracellular staining by Gp-anti-TRPV1 hints at a splice variant because this splicing affects translocation to the membrane (Hellwig et al 2005).…”

Section: Discussionmentioning

confidence: 98%

“…Indeed, the effects of TRPV1 on GI functioning have mostly been linked to its expression in extrinsic nerve fibers. Regardless of GI region or species, TRPV1 is widely known to be expressed in afferent nerve fibers (Guo et al 1999;Yiangou et al 2001;Poonyachoti et al 2002;Anavi-Goffer and Coutts 2003;Chan et al 2003;De Jonge et al 2003;Ward et al 2003;Schicho et al 2004;Kadowaki et al 2004;Faussone-Pellegrini et al 2005;Matsumoto et al 2011). Some of these studies also reported an intrinsic expression of TRPV1 in the GI tract of several mammalian species (Akiba et al 2001;Kulkarni-Narla and Brown 2001;AnaviGoffer et al 2002;Poonyachoti et al 2002;Anavi-Goffer and Coutts 2003;Chan et al 2003;Faussone-Pellegrini et al 2005), as further corroborated by a physiological study in the mouse by Penuelas et al (2007).…”

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confidence: 84%

Transient Receptor Potential Vanilloid Type 1 Channel (TRPV1) Immunolocalization in the Murine Enteric Nervous System Is Affected by the Targeted C-terminal Epitope of the Applied Antibody

Buckinx

Nassauw

Avula

et al. 2013

J Histochem Cytochem.

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The expression of transient receptor potential vanilloid type 1 channel (TRPV1) in the enteric nervous system is still the subject of debate. Although a number of studies have reported that TRPV1 is limited to extrinsic afferent fibers, other studies argue for an intrinsic expression of TRPV1. In the present study, reverse transcriptase PCR was employed to establish the expression of TRPV1 mRNA throughout the gastrointestinal tract. Using two antibodies directed against different epitopes of TRPV1, we were able to show at the protein level that the observed distribution pattern of TRPV1 is dependent on the antibody used in the immunohistochemical staining. A first antibody indeed mainly stained neuronal fibers, whereas a second antibody exclusively stained perikarya of enteric neurons throughout the mouse gastrointestinal tract. We argue that these different distribution patterns are due to the antibodies discriminating between different modulated forms of TRPV1 that influence the recognition of the targeted immunogen and as such distinguish intracellular from plasmalemmal forms of TRPV1. Our study is the first to directly compare these two antibodies within the same species and in identical conditions. Our observations underline that detailed knowledge of the epitope that is recognized by the antibodies employed in immunohistochemical procedures is a prerequisite for correctly interpreting experimental results.

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“…The specimens were immediately immersed in 4% paraformaldehyde in 0.1 M phosphate buffer (pH 7.0) at room temperature. After a 10-min fixation period, the DRG were processed for cryosectioning according to published methods (9). To assess the presence of TRPV1 in spinal neurons, cryostat sections were immunocytochemically stained with a rabbit antibody directed against TRPV1 (AB5370; CHEMICON International, Temecula, CA; diluted 1:400) and a Cy3-conjugated goat anti-rabbit IgG (Jackson Immunoresearch Laboratories, West Grove, PA; diluted 1:4,000).…”

Section: Methodsmentioning

confidence: 99%

TRPV1 receptor signaling mediates afferent nerve sensitization during colitis-induced motility disorders in rats

Schepper¹,

Man²,

Ruyssers³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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BY. TRPV1 receptor signaling mediates afferent nerve sensitization during colitis-induced motility disorders in rats. Am J Physiol Gastrointest Liver Physiol 294: G245-G253, 2008. First published November 8, 2007 doi:10.1152/ajpgi.00351.2007.-Rats with experimental colitis suffer from impaired gastric emptying (GE). We previously showed that this phenomenon involves afferent neurons within the pelvic nerve. In this study, we aimed to identify the mediators involved in this afferent hyperactivation. Colitis was induced by trinitrobenzene sulfate (TNBS) instillation. We determined GE, distal front, and geometric center (GC) of intestinal transit 30 min after intragastric administration of a semiliquid Evans blue solution. We evaluated the effects of the transient receptor potential vanilloid type 1 (TRPV1) antagonists capsazepine (5-10 mg/kg) and N- (4-tertiarybutylphenyl)-4-(3-cholorphyridin-2-yl)tetrahydropyrazine-1(2H)carboxamide (BCTC; 1-10 mg/kg) and the calcitonin generelated peptide (CGRP) receptor antagonist CGRP-(8-37) (150 g/ kg). To determine TRPV1 receptor antagonist sensitivity, we examined their effect on capsaicin-induced relaxations of isolated gastric fundus muscle strips. Immunocytochemical staining of TRPV1 and RT-PCR analysis of TRPV1 mRNA were performed in dorsal root ganglion (DRG) L6 -S1. TNBS-induced colitis reduced GE but had no effect on intestinal motility. Capsazepine reduced GE in controls but had no effect in rats with colitis. At doses that had no effects in controls, BCTC and CGRP-(8-37) significantly improved colitis-induced gastroparesis. Capsazepine inhibited capsaicininduced relaxations by 35% whereas BCTC completely abolished them. TNBS-induced colitis increased TRPV1-like immunoreactivity and TRPV1 mRNA content in pelvic afferent neuronal cell bodies in DRG L6 -S1. In conclusion, distal colitis in rats impairs GE via sensitized pelvic afferent neurons. We provided pharmacological, immunocytochemical, and molecular biological evidence that this sensitization is mediated by TRPV1 receptors and involves CGRP release. gastric emptying; sensory nerve; pelvic nerve; CGRP PATIENTS WITH INFLAMMATORY bowel disease (IBD) often suffer from disorders of gastrointestinal motility and sensitivity, imposing a significant load on the patient's quality of life (20). These alterations are known to appear both during inflammatory episodes and in periods of remission and can occur either at the site of inflammation or at a distance from this site (43). Especially concerning the latter situation, little is known about the underlying pathophysiological mechanisms. There have been several studies documenting the effects of isolated experimental colitis on small intestinal neuromuscular function, but the in vivo consequences on gut transit were inconclusive (3, 5, 29). McHugh et al. (37) reported that rats with trinitrobenzene sulfate (TNBS)-induced colitis suffer from a reduction of gastric emptying but did not investigate the underlying mechanisms. We recently confirmed that rats with experimental...

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Effect of intestinal inflammation on capsaicin-sensitive afferents in the ileum of Schistosoma mansoni -infected mice

Cited by 50 publications

References 38 publications

Protective Effect of Proteinase-Activated Receptor 2 Activation on Motility Impairment and Tissue Damage Induced by Intestinal Ischemia/Reperfusion in Rodents

Protective Effect of Proteinase-Activated Receptor 2 Activation on Motility Impairment and Tissue Damage Induced by Intestinal Ischemia/Reperfusion in Rodents

Transient Receptor Potential Vanilloid Type 1 Channel (TRPV1) Immunolocalization in the Murine Enteric Nervous System Is Affected by the Targeted C-terminal Epitope of the Applied Antibody

TRPV1 receptor signaling mediates afferent nerve sensitization during colitis-induced motility disorders in rats

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